Etiologic factors in femoral head osteonecrosis in growing rats

Suehiro, Masatsugu; Hirano, Tôru; Mihara, Keiji; Shindo, Hiroyuki

doi:10.1007/s007760050008

Cited by 18 publications

(4 citation statements)

References 12 publications

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“…Also, if the SHRs are placed on a restricted diet (leading to a reduction in body weight), there is a significant drop in the frequency of Perthes' characteristics (Tomita et al, ; Kawahara et al, ), presumably because they overload their hips less. If the ordinary WKYs are forced to stand on their hind legs when feeding, thereby overloading their hip joints, they develop features of Perthes' at a frequency similar to the SHRs (Suehiro et al, ). Thus, it appears that, although there is a genetic factor that increases levels of susceptibility of Perthes' disease in nonhuman animals, biomechanical overloading of the hip joint appears to be the trigger which causes Perthes' disease.…”

Section: Perthes' Disease In Nonhuman Animalsmentioning

confidence: 99%

Skeletal immaturity, rostral sparing, and disparate hip morphologies as biomechanical causes for Legg‐Calvé‐Perthes' disease

et al. 2016

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Legg-Calvé-Perthes' (Perthes') disease is a developmental disease of the hip joint that may result in numerous short and long term problems. The etiology of the disease remains largely unknown, but the mechanism is believed to be vascular and/or biomechanical in nature. There are several anatomical characteristics that tend to be prevalent in children with Perthes' disease, namely: skeletal immaturity, reduced height, and rostral sparing. We present an overview of the literature, summarizing the current understanding of the pathogenesis, particularly related to how the formation of the vasculature to the femoral epiphysis places children aged 5-8 at a higher risk for Perthes' disease, how skeletal immaturity and rostral sparing could increase the probability of developing Perthes' disease, and how animal models have aided our understanding of the disease. In doing so, we also explore why Perthes' disease is correlated to latitude, with populations at higher latitudes having higher incidence rates than populations closer to the Equator. Finally, we present five hypotheses detailing how Perthes' disease could have a biomechanical cause. Clin. Anat. 29:759-772, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Perthes' Disease In Nonhuman Animalsmentioning

confidence: 99%

Skeletal immaturity, rostral sparing, and disparate hip morphologies as biomechanical causes for Legg‐Calvé‐Perthes' disease

et al. 2016

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“…Mechanical stress-induced ischemia was found to be a possible aetiology of LCPD also using several animal models[70-72] and experimental analysis models[65,73,74]. One particular study performed by Suehiro et al[49] involving Wistar Kyoto rats reported how repetitive mechanical stress on the femoral heads from 5 wk to 9 wk of age played an important role in the aetiology of osteonecrosis.…”

Section: Resultsmentioning

confidence: 99%

Aetiology of Legg-Calvé-Perthes disease: A systematic review

Pavone

Chisari

Vescio

et al. 2019

WJO

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BACKGROUNDLegg-Calvé-Perthes disease (LCPD) is a clinical condition affecting the femoral head of children during their growth. Its prevalence is set to be between 0.4/100000 to 29.0/100000 children less than 15 years of age with a peak of incidence in children aged from 4 years to 8 years. LCPD aetiology has been widely studied, but it is still poorly understood.AIMTo analyse the available literature to document the up-to-date evidence on LCPD aetiology.METHODSA systematic review of the literature was performed regarding LCPD aetiology, using the following inclusion criteria: studies of any level of evidence, reporting clinical or preclinical results and dealing with the aetiology or pathogenesis of LCPD. Two reviewers searched the PubMed and Science Direct databases from their date of inception to the 20th of May 2018 in accordance with the Preferred Reporting Items for Systemic Reviews and Meta-Analyses guidelines. To achieve the maximum sensitivity of the search strategy, we combined the terms: ‘‘Perthes disease OR LCPD OR children avascular femoral head necrosis” with “pathology OR aetiology OR biomechanics OR genetics” as either key words or MeSH terms.RESULTSWe include 64 articles in this review. The available evidence on LCPD aetiology is still debated. Several hypotheses have been researched, but none of them was found decisive. While emerging evidence showed the role of environmental risk factors and evidence from twin studies did not support a major role for genetic factors, a congenital or acquired predisposition cannot be excluded in disease pathogenesis. One of the most supported theories involved mechanical induced ischemia that evolved into avascular necrosis of the femoral head in sensible patients.CONCLUSIONThe literature available on the aetiology of LCPD presents major limitations in terms of great heterogeneity and a lack of high-profile studies. Although a lot of studies focused on the genetic, biomechanical and radiological background of the disease, there is a lack of consensus on one or multiple major actors of the etiopathogenesis. More studies are needed to understand the complex and multifactorial genesis of the avascular necrosis characterizing the disease.

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“…Namely, oxidative injury, which is thought to be a cause of osteonecrosis, is associated with an especially intraosseous susceptibility to mitochondrial injury, suggesting that mechanical stress due to loading is one cause. In practice, when mechanical stress is imposed on the femur the proportion of osteonecrosis increases 12 13 , while decreasing the amount of mechanical stress has been found to make possible reduction of this causative factor of femoral head necrosis. Furthermore, as accumulation of oxidative stress due to excessive free radical production induced by mechanical stress has also been reported 14 , the femur and humerus can be considered tissues exposed to excessive stress from the start making them especially vulnerable when then subjected to overload as well.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial stress and redox failure in steroid-associated osteonecrosis

Tsuchiya¹,

Ichiseki²,

Ueda³

et al. 2018

Int. J. Med. Sci.

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The purpose of the role of antioxidant enzymes and mitochondria in the developmental mechanism of steroid-associated osteonecrosis in the femur. In the present study Japanese white rabbits (mean weight 3.5kg) were injected into the gluteus with methylprednisolone (MP) 20mg/kg, and killed after 3 days (MP3 group), 5 days (MP5 group), and 14 days (MP14 group) (n=3 each). As a Control group (C group) Japanese white rabbits not administered MP were used. In experiment 1, the expression of the antioxidant enzymes Superoxide dismutade (SOD) and catalase was compared in liver, kidney, heart, humerus, and femur in C group, and the presence/absence of mitochondria transcription factor A (TFAM) expression was determined by Western blotting (WB) and used to evaluate the number of mitochondria and their function. In experiment 2, the presence/absence of necrosis was determined by immunohistochemistry, while changes in the expression of SOD, catalase, and TFAM in the femur after steroid administration were determined by Western blotting (WB). In experiment 1, intense expression of all of SOD, catalase, and TFAM was found in the liver, kidney, and heart as compared to the humerus and femur. In experiment 2, the expression of all of SOD, catalase, and TFAM in MP3 and MP5 groups was decreased on WB as compared with C group, while in MP14 group a tendency to improvement was seen. Accordingly, steroid-associated mitochondrial injury and redox failure are concluded to be important elements implicated in the pathogenesis of osteonecrosis.

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Etiologic factors in femoral head osteonecrosis in growing rats

Cited by 18 publications

References 12 publications

Skeletal immaturity, rostral sparing, and disparate hip morphologies as biomechanical causes for Legg‐Calvé‐Perthes' disease

Skeletal immaturity, rostral sparing, and disparate hip morphologies as biomechanical causes for Legg‐Calvé‐Perthes' disease

Aetiology of Legg-Calvé-Perthes disease: A systematic review

Mitochondrial stress and redox failure in steroid-associated osteonecrosis

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